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PubMedDate not supplied

[Role of the hypothalamus in the regulation of primary sleep in the frog Rana temporaria].

It has been demonstrated that in the frog Rana temporaria the anterior hypothalamus is involved into regulation of the depth of two forms of rest--one with plastic, the other with decreased muscle tone. Resting state with catatonic muscle activity is associated with activation of the posterior hypothalamus. Participation of the anterior hypothalamus in regulation of the resting state with the decreased tone of skeletal muscles may be taken as one of the indications that this form of rest plays the role of sleep in amphibians, being transformed during evolution of vertebrates into the sleep of poikilotherms.

Animals↗
PubMed1975

[Influence of the anterior and posterior hypothalamus on the conditioned reflex activity and delayed responses of lower simians].

In 4 adult monkeys, electrical stimulation of the anterior hypothalamus followed by subsidence in the animal and the ECoG synchronization evoked also an impairment of conditioned reflex activity and a decrease in the test performance during delayed responses. Strong stimulation of the posterior hypothalamus followed by emotional arousal and desynchronization in the ECoG, on the contrary, improved the conditioned reflex activity and increased the level of the test performance. The hypothalamus is then supposed to play a certain role in memory as an emotiogenic structure.

Animals↗
PubMed1976

The diencephalon of the vervet monkey (Cercopithecus aethiops). Part II: epithalamus, subthalamus and hypothalamus.

The nuclear configuration and topography of the epithalamus, subthalamus and hypothalamus of the vervet monkey (Cercopithecus aethiops) are described and compared with those of other primates, particularly the macaque monkey. The epithalamus does not show any striking structural differences, except some architectonic differentiation in the lateral habenular nucleus. The subthalamus is a phylogenetically stable structure throughout the primate scale; it does not show any significant changes, except that it extends less rostrally and that the nuclei entopeduncularis and peripeduncularis are much smaller and less well defined in the vervet monkey than those in the diencephalon of lower primates. The nucleus subthalamicus and the fields of Forel, though small in size, are comparatively well developed; the zona incerta appears to be differentiated cytoarchitectonically into two parts. The hypothalamus is divided morphologically into four regions--the preoptic, supraoptic, infundibular and mamillary regions. Although the hypothalamus of the vervet monkey is topographically identifiable with those of other primates, there are cyto- and myeloarchitectonic differences to be found in certain hypothalamic nuclei and areas. The preoptic region is small and poorly delimited from the parolfactory region antierorly and the supraoptic region posteriorly. The nucleus paraventricularis is large and well differentiated into secretory and non-secretory portions; the nucleus supraopticus does not show cellular separation into dorsolateral and ventromedial parts as clearly as they are in other primates. The nucleus dorsomedialis is not as well defined as the nucleus ventromedialis like it is in other primates. The nucleus tuberalis lateralis is comparably small, and is not split into several cellular groups as it is in higher primates. The posterior hypothalamic area is morphologically the best definable of the hypothalamic areas. The mamillary region is developmentally advanced, and very well differentiated into medial, lateral and intercalated nuclei.

Animals↗
PubMed1977

[Effect of polypeptides isolated from the anterior hypothalamus and epiphysia on cells of the hypothalamo-hypophyseal neurosecretory system].

A comparative study on the influence of physiologically active substances, extracted from the epiphysis and the anterior hypophalamus, on the morpho-functional status of the cells of the hypophalamo hypophysial neurosecretory system was carried out. The substances in question were extracted from the cattie epiphysis and anterior hypothalamus by means of acetic acid extraction from acetone-dehydrated tissue and the following sedimentation of the substances by means of cooled acetone and lyophilization. The investigation of the substances demonstrated them to be polypeptides with an average molecular weights from 2.000 to 10.000. The experiment was done in male rats Wistar strain Morphofunctional status of the hypothalamo-hypophysial neurosecretory system was estimated in paraffin sections, stained with paraldehyde-fuchsine after Gomori- Gabe and additional staining with azan after Heidenhain. The data obtained demonstrated that injection of the substances excreted by the anterior hypothalamus and epiphysis produced opposite changes in the functional status of the cells of the hypothalamo-hypophysial neurosecretory system: the substances from the epiphysis increased, while the substances from the hypothalamus, on the contrary, decreased their activity.

Animals↗
PubMed1988

Local synaptic organization of cholinergic neurons in the basolateral hypothalamus.

A monoclonal antibody to choline acetyltransferase (ChAT) was utilized for immunocytochemical identification of cholinergic neurons in the basolateral hypothalamus. Light and electron microscopic examination revealed a network of cell bodies, dendrites, and axonal processes dorsolateral to the supraoptic nucleus. Within this region the cells immunoreactive for ChAT receive numerous unlabeled terminals which contact dendrites, cell soma, axons and occasional somatic spines. In a few cases, small ChAT-immunoreactive terminals were observed contacting a cholinergic cell soma or large dendrite. Many ChAT-immunoreactive fibers were directed toward the supraoptic nucleus forming a dense local network but very few of these fibers penetrated deeper than approximately 20 micron into the supraoptic nucleus. A total of 63 ChAT-immunoreactive terminals were mapped within the basal hypothalamus, of which the vast majority contacted unlabeled dendrites immediately dorsolateral to the supraoptic nucleus. Labeled terminals were rare or nonexistent in the medial portions of the hypothalamus or deep within the supraoptic nucleus. This pattern of ChAT terminal densities correlates with the distribution of binding for the muscarinic cholinergic probe, [3H]quinuclidinylbenzilate, but not the binding of the putative nicotinic cholinergic probe, [125I]alpha-bungarotoxin, which is high within the supraoptic nucleus. Thus, the cholinergic neurons of the basal hypothalamus appear to form a network of intrinsic connections which probably represent input to muscarinic cholinergic receptors. No evidence was found to suggest that cholinergic presynaptic terminals were colocalized with the alpha-bungarotoxin binding protein within the supraoptic nucleus.

Animals↗
PubMed1993

Reactive astrocytes involved in the formation of lesional scars differ in the mediobasal hypothalamus and in other forebrain regions.

The fine organization of lesional scars was studied in adult rats at the level of 2 types of surgical cuts aimed at deafferentating the dorsal hypothalamus from its neuropeptide-Y innervation. These included: (i) lesions located dorsolateral to the dorsal hypothalamus, which were shown to form a permanent obstacle to the regeneration of transected neuropeptide-Y-fibers, and (ii) lesions located in the ventromedial hypothalamus, where transected neuropeptide-Y-fibers were shown to penetrate and eventually cross the lesional area. Double labeling immunocytochemistry and conventional electron microscopy were used to identify various molecules produced by reactive astrocytes and to visualize their ultrastructural organization within the scars, respectively. In the different portions of the dorsolateral scars, the large majority of reactive astrocytes was characterized by a strong immunoreactivity to glial fibrillary acidic protein, vimentin, and embryonic (polysialylated) NCAM. Intense laminin-immunoreactivity was also observed over large patches included in the scar. Electron microscope observations further indicated that the matrix of the scar was mainly composed of tightly packed astrocytic perikarya and processes connected by extended gap junctions. All around the extracellular and perivascular spaces, these astrocyte profiles were bordered by a thick basal lamina. Only scarce axonal profiles were detected in the core of the scar, most of which exhibited degenerative features. In the ventromedial hypothalamic scars, reactive astrocytes were found to exhibit intense immunoreactivity to both glial fibrillary acidic protein and vimentin. On the other hand, only slight immunostaining to embryonic NCAM and laminin were associated with this type of lesional scar. At the ultrastructural level, the main differences with the dorsolateral scars concerned (i) the gap junctions, which were less frequent and involved shorter portions of adjacent membranes; (ii) the basal lamina, which was essentially localized to the perivascular spaces; and (iii) the axonal profiles, which were frequently observed throughout the scar matrix. These data indicate that reactive astrocytes that formed the glial scar differ in the mediobasal hypothalamus and in other forebrain regions. This provides strong support for the hypothesis that the regeneration of neuropeptide-Y axons through a mediobasal hypothalamic surgical cut depends mainly on the particular organization of the astroglial scar.

Animals↗
PubMed1998

Tanycytes present in the adult rat mediobasal hypothalamus support the regeneration of monoaminergic axons.

We have recently shown that tanycytes present in the median eminence (ME) constitute a preferential support for the regeneration of lesioned neurohypophysial oxytocinergic and vasopressinergic axons. However, although tanycytes are particularly abundant in the ME, they are also present along the third ventricle wall. This study was thus undertaken to determine whether tanycytes present in the mediobasal hypothalamus overlying the ME were also able to support the regeneration of the numerous monoaminergic axons innervating this region. Using confocal laser scanning microscopy combined with double or triple fluorescence immunostaining, we have compared the relationships occurring between glial cells and lesioned catecholaminergic and serotonergic axons at the levels of surgical cuts placed in the dorsomedial hypothalamus devoid of tanycytes or in the ventromedial hypothalamus containing numerous tanycyte processes. In dorsal lesions, catecholaminergic and serotonergic transected fibers were found to abut onto the scar formed along the surgical cut and composed of closely inderdigitating astrocyte processes strongly immunoreactive for both glial fibrillary acidic protein (GFAP) and vimentin (VIM). In ventral lesions, the lesional scar was composed of GFAP-immunoreactive (IR) and VIM-IR astrocyte processes and of VIM-IR but GFAP-negative processes that were identified as tanycytic processes. In all the ventral lesions examined, numerous catecholaminergic and serotonergic fibers were found to regenerate into the surgical cut in association with the VIM-IR, GFAP-negative tanycyte processes. On the other hand, such regenerating fibers were never found in scar portions containing only GFAP-IR astrocytic structures. These data indicate that, like in the ME, tanycytes present in the mediobasal hypothalamus of adult rat provide a substrate that favors the regeneration of lesioned axons.

Age Factors↗
PubMed1999

Different distributions of nitric oxide synthase-containing neurons in the mouse and rat hypothalamus.

The distribution of nitric oxide synthase-containing neurons was studied in the rat and mouse hypothalamus by immunohistochemistry and NADPH-diaphorase histochemistry. Immunostaining and NADPH-diaphorase staining of hypothalamic neurons were comparable in all hypothalamic nuclei of either species except in the arcuate nucleus that stained positive for nitric oxide synthase immunoreactivity but negative for NADPH-diaphorase reactivity. The presence of nitric oxide synthase-immunopositive neurons in the arcuate nucleus was confirmed by nitric oxide synthase immunofluorescence viewed under the confocal microscope at 1 microm thickness. Cross-species comparison showed that, in general, the number and intensity of nitric oxide synthase-containing neurons were much higher in the rat than in the mouse hypothalamus. Differences in the distribution of nitric oxide synthase-containing neurons between these two rodents were found in most hypothalamic nuclei. In particular, two dense clusters of nitric oxide synthase-containing neurons were found in the paraventricular and supraoptic nuclei of the rat hypothalamus in contrast to their scarcity in the same nuclei of the mouse hypothalamus.

Animals↗
PubMed1992

N-methyl-D-aspartate lesions of the lateral hypothalamus do not reduce amphetamine or fenfluramine anorexia but enhance the acquisition of eating in response to tail pinch in the rat.

These experiments examine the acquisition of tail pinch-induced eating and responses to the anorectic agents d-amphetamine and d,l-fenfluramine by rats bearing N-methyl-D-aspartate (NMDA) lesions of the lateral hypothalamus. Lesioned rats lost weight following surgery but had no significant eating or drinking difficulties in the home cage (Clark et al. 1990). The acquisition of eating in response to tail pinch was enhanced in lateral hypothalamic-lesioned rats: they ate on earlier test sessions than controls and less pressure was required to elicit eating. Home cage food intake over the period when tail pinch was being examined was not affected by the lateral hypothalamic lesions. There were no significant differences between lateral hypothalamic-lesioned and control rats in terms of their anorectic responses to either d-amphetamine or d,l-fenfluramine, though the lesioned rats had a lower baseline intake. These data suggest that the lateral hypothalamus is not an important site for the mediation of amphetamine or fenfluramine anorexia but is involved in the acquisition of tail pinch-induced eating. The disinhibition of responding to tail pinch by lateral hypothalamic lesions is discussed in terms of the possible role the lateral hypothalamus plays in regulating cortical activity. The role of the medial hypothalamus and non-hypothalamic systems in the response to anorectic drugs and tail pinch is discussed.

Amphetamine↗
PubMedDate not supplied

Effect of stimulation of the lateral hypothalamus on the correlation of neuron spike activity in the rabbit neocortex.

Cross-correlation and autocorrelation histograms were constructed with the aim of studying correlated spike activity of neurons in the visual and sensorimotor regions of both hemispheres of the rabbit brain before and after stimulation of the right and left lateral hypothalamic regions, which generates food-motivated responses. Stimulation of the left hypothalamus produced larger rearrangements in correlated neuron firing than stimulation of the right hypothalamus. Stimulation of the left hypothalamus, unlike that of the right hypothalamus, was followed by significant increases in the numbers of pairs of left hemisphere neocortical neurons with linked activity, and also induced the sequential firing of neurons in a particular defined order: sensorimotor cortex cells fired first, followed by visual cortex neurons after delays of up to 120 msec. It is concluded that cortical interhemisphere asymmetry in conditions of hunger is associated with nonuniform functioning of the right and left lateral hypothalamic regions.

Animals↗
PubMed1986

Destruction of intrinsic neurons in the lateral hypothalamus disrupts the classical conditioning of autonomic but not behavioral emotional responses in the rat.

The present study examined whether destruction of intrinsic neurons in the lateral hypothalamus of the rat would disrupt the acquisition of classically conditioned changes in arterial pressure. Ibotenic acid, a cellular toxin which spares axons of passage, was injected bilaterally in the hypothalamus either medial or lateral to the fornix. After 2 weeks the animals were subjected to classical fear conditioning trials involving the presentation of a tone in association with footshock. The next day changes in arterial pressure and emotional behavior elicited by the tone alone were measured. Destruction of intrinsic neurons in the lateral hypothalamus prevented the normal establishment of the arterial pressure conditioned response but did not affect the behavioral response. Unconditioned arterial pressure responses elicited by the tone and shock were not affected. Medial hypothalamic injections had no effect on any of the responses. The location of the lateral hypothalamic cell loss overlapped with the neurons projecting to the autonomic region of the spinal cord. Intrinsic neurons in the lateral hypothalamus therefore appear to be specifically involved in mediating learned cardiovascular adjustments.

Animals↗
PubMed1993

Where does damage lead to enhanced food aversion: the ventral pallidum/substantia innominata or lateral hypothalamus?

It is well known that lesions of the lateral hypothalamus (LH) produce aphagia. Several previous studies have reported that lateral hypothalamus damage produces food aversion in addition to aphagia. However, damage to other regions near the LH also produce aphagia and enhanced aversion. The purpose of this study was to resolve where the site or sites for aversion-inducing lesions is/are located. Small, bilateral excitotoxin lesions (QUIN, 10 micrograms in 1 microliter or IBO, 15 micrograms in 1 microliter) or bilateral sham injections of vehicle were made into the globus pallidus (GP), the ventral pallidum/substantia innominata (VP/SI) or the lateral hypothalamus (LH). Affective reactions to taste were elicited by infusing sucrose solutions (1 M) into the mouth via chronic oral cannulae. The number of aversive responses (gapes, chin-rubbing, head-shaking and forelimb flails) emitted was tallied. Individual lesions were mapped and a single 'necessary and sufficient' site for damage-induced aversion was identified (the area of overlapping damage common to all rats that showed enhanced aversive reactions). To identify the lesions, two lesion-mapping techniques were used: (1) a conventional neuron-counting procedure in which an attempt is made to count all neurons within a brain region, and (2) a new modified 'fractionator' procedure consisting of exhaustive 400 x magnification counts at point locations within a brain region. Results indicated that aversive reactions to food are enhanced only following bilateral neuron loss (> 70%) from the caudal ventromedial VP/SI alone. This shared site has a lateral diameter of 1.0 mm, a dorsoventral diameter of 0.5 mm and a rostrocaudal diameter of 1.0 mm. Damage restricted to the LH never produced enhanced aversion even when it produced aphagia. The crucial region for aversion is located ventral and medial to the globus pallidus and dorsal and lateral to the lateral hypothalamus.

Animals↗
PubMed1995

Differential expression of vasopressin receptor binding in the hypothalamus during lactation in golden hamsters.

Vasopressin (AVP) receptor binding within hypothalamic sites was compared between cycling and lactating female golden hamsters. The density of AVP receptor binding was analyzed by quantitative autoradiography within the ventrolateral hypothalamus and dorsomedial hypothalamic nucleus. Lactation was correlated with a disappearance of AVP receptor binding within the ventrolateral hypothalamus. In contrast, lactation was associated with a two- to three-fold increase in the density of AVP receptor binding within the dorsomedial hypothalamic nucleus. These results suggest that AVP receptor binding within the ventrolateral hypothalamus is responsive to gonadal hormones in female golden hamsters. However, the increase in binding observed within the dorsomedial hypothalamus may be related to other neurobiological changes associated with lactation.

Animals↗
PubMed1991

Oxytocin effects on lordosis frequency and lordosis duration following infusion into the medial pre-optic area and ventromedial hypothalamus of female rats.

When infused into the medial preoptic area of ovariectomized female rats treated with estradiol benzoate (3 micrograms) and progesterone (150 micrograms), oxytocin was found to increase the lordosis frequency and the lordosis duration. Oxytocin administered into the ventromedial hypothalamus increased the lordosis duration but not the lordosis frequency. In the mesencephalic central grey, oxytocin did not significantly affect lordosis. Oxytocin in the ventromedial hypothalamus facilitated lordosis duration at doses which were ineffective in the medial preoptic area. This contrasts with the pattern of results observed for lordosis frequency. These results lend support to the hypothesis that the lordosis-facilitating actions of oxytocin in the ventromedial hypothalamus are due to a permissive effect of progesterone and that the ventromedial hypothalamus and medial pre-optic area may control different aspects of lordosis.

Animals↗
PubMed1984

Injections of phentolamine into the anterior hypothalamus-preoptic area of rats blocks both pressor and drinking responses produced by central administration of angiotensin II.

There are conflicting reports of a possible contribution of noradrenergic projections to the rostral hypothalamus to drinking and blood pressure regulation. The present study investigated the effects of injecting phentolamine into the anterior hypothalamus-preoptic region on drinking and blood pressure responses elicited by injecting angiotensin II into a lateral cerebral ventricle of the rat. Angiotensin II (250 ng or 25 ng) elicited water intakes averaging 9.25 +/- 0.52 ml and 4.35 +/- 0.44 ml respectively in 15 min with latencies of less than 3 min. Phentolamine, an alpha-adrenergic antagonist, injected into the rostral hypothalamus produced a dose-dependent reduction in water intake and number of laps taken accompanied by an increased latency to drink. In the urethane anaesthetized rat, angiotensin II produced significant increases in blood pressure. Injections of phentolamine into rostral hypothalamic sites in which drinking responses to angiotensin II were attenuated, also attenuated the pressor response to angiotensin II. These results indicate that alpha-adrenergic input to the rostral hypothalamus is involved in both the pressor and drinking responses elicited by central angiotensin II.

Angiotensin II↗
PubMed1989

Evidence for the presence of PNMT-containing cell bodies in the hypothalamus.

The presence of intrinsic neurons in the hypothalamus containing the enzyme phenylethanolamine N-methyltransferase (PNMT), was investigated by selective destruction of the local cell bodies with kainic acid (KA), a potent excitotoxin. The unilateral stereotaxic injection of 2 micrograms of KA into the lateral hypothalamus produced a 30-35% decrease in the hypothalamic PNMT activity in the lesioned side compared with the contralateral uninjected side. The difference was statistically significant for up to 4 days after the lesion. The unilateral lesion did not have a unilateral effect on epinephrine or norepinephrine content as there was a significant reduction on both sides (50% for epinephrine and 30% for norepinephrine compared with saline injected). These data suggest the presence of intrinsic cell bodies in the lateral hypothalamus, containing the epinephrine-forming enzyme but lacking epinephrine storage sites. Our results support the previous hypothesis of the dissociation between epinephrine present in the hypothalamus and hypothalamic PNMT activity.

Animals↗
PubMed2003

Alterations in hypothalamic-pituitary-adrenal axis activity and in levels of proopiomelanocortin and corticotropin-releasing hormone-receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' cocaine and withdrawal.

Tolerance to the stimulatory effects of cocaine on the hypothalamic-pituitary-adrenal (HPA) axis develops after chronic 'binge' cocaine exposure in the rat. This blunting of HPA axis activity in response to cocaine is associated with a cocaine-induced reduction of corticotropin-releasing hormone (CRH) mRNA level in the hypothalamus. There is limited information about the effects of withdrawal from chronic cocaine on HPA activity. The present studies were undertaken to determine levels of the HPA hormones adrenocorticotropic hormone (ACTH) and corticosterone across 10 days of withdrawal following chronic 'binge' pattern cocaine administration (3 x 15 mg/kg/day at hourly intervals) for 14 days. Male Fischer rats showed a significantly attenuated HPA axis response to chronic 'binge' pattern cocaine administration 30 min after the last injection on the 14th day, as measured by both plasma ACTH and corticosterone levels at the nadir time point. Twenty-four hours following the final administration of 'binge' cocaine (the 1st day of withdrawal), a significant elevation of plasma ACTH levels and a modest, but significant, elevation of plasma corticosterone levels were found at the nadir time point. This acute withdrawal-related activation of the hormones of the HPA axis was no longer found on the 10th day of withdrawal. In the anterior pituitary, levels of both proopiomelanocortin (POMC) and CRH-receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' cocaine and were at control levels on the 4th day of withdrawal. In the neurointermediate lobe of the pituitary, a sustained reduction in POMC mRNA levels was observed on the 3rd, 7th and 14th day of chronic 'binge' cocaine, but POMC mRNA was at control levels by the 4th day of withdrawal. In the hypothalamus, POMC mRNA levels showed a transient decrease on the 1st day of 'binge' cocaine with no change during chronic 'binge' cocaine or its withdrawal. CRH mRNA levels in the hypothalamus were not different from saline controls on the 1st and 4th days of withdrawal. Taken together, the present results show that after development of adaptation or tolerance to chronic 'binge' cocaine there is an increase in HPA activity during acute cocaine withdrawal. In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or CRH-R1 gene expression observed in the anterior pituitary after chronic 'binge' cocaine.

Adrenal Glands↗
PubMed1997

Lesions of the ventromedial hypothalamus reduce postingestional thermogenesis.

The aim of this experiment was to evaluate the effects of ventromedial hypothalamus lesions on the thermogenic changes that follow food intake. Four groups of six Sprague-Dawley male rats were used. Under anesthesia with pentobarbital, the animals in the first and second groups received lesions at the ventromedial hypothalamus, and animals in the third and fourth groups received sham lesions. Body weight and food intake were monitored daily until the experimental procedure began. Twenty days after lesion, oxygen consumption, firing rate of sympathetic nerves to interscapular brown adipose tissue (IBAT), and IBAT temperature were monitored for 45 min both before and after 5 g food intake in 24 h fasted rats from the first and third groups. The same variables were measured in the animals of the second and fourth groups 50 days after receiving the lesions. Lesion placements were histologically verified. The results showed that lesions produced hyperphagia and obesity. Firing rate of nerves to IBAT, IBAT temperature, and oxygen consumption increased after food intake in sham-lesioned rats. This increase was significantly reduced by the lesion at both the 20- and 50-day time points. These findings indicate that the ventromedial hypothalamus controls postingestional activation of sympathetic discharge to IBAT. The reduction of postingestional thermogenesis could be involved in the development of obesity induced by lesion of the ventromedial hypothalamus.

Adipose Tissue, Brown↗